Ac2-26 TFA, an active N-terminal peptide of annexin A1 (AnxA1), attenuates ischemia-reperfusion-induced acute lung injury. Ac2-26 also decreases AnxA1 protein expression, inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue.
This is a hypoxia-inducible factor-1 (HIF-1 a) 19-mer fragment. HIF-1 functions as master regulator of response to oxygen homeostasis. Hypoxia-induced gene expression is initiated when HIF-1 subunit is stabilized in response to a lack of oxygen. This part
N-Acetyl-Ser-Asp-Lys-Pro (TFA) is an endogenous tetrapeptide that is naturally produced in the bone marrow. It serves as a specific substrate for the N-terminal site of ACE, the enzyme responsible for angiotensin converting activity.
Endogenous potent and highly selective bradykinin B1 receptor agonist (Ki values are 0.12 and > 30000 nM at human B1 and B2 receptors respectively). Hypotensive agent that reduces peripheral vascular resistance in vivo. 16-fold more potent than [Des-Arg9]
Chemerin-9 (149-157) TFA, the nonapeptide (149)YFPGQFAFS(157) (chemerin-9), corresponding to the C terminus of processed chemerin, retains most of the activity of the full-size protein, with regard to agonism toward the chemerinR[1].
TP508 TFA is a nonproteolytic thrombin peptide. TP508 TFA activates endothelial NO synthase (eNOS) and stimulates the production of NO in human endothelial cells. It activates endothelial cells and stem cells to revascularize and regenerates tissues.
LCMV gp33-41 (TFA), the carboxyl-extended 11-aa-long peptide, is an lymphocytic choriomeningitis virus sequence restricted by MHC class I H-2Db molecules and presented to cytotoxic T lymphocytes[1].
Lactoferrin (17-41) TFA (146897-68-9 free base) is amino acids 17 to 41 fragment of lactoferrin, known as lactoferricin B. Lactoferrin (17-41) TFA (146897-68-9 free base) shows anti-fungal properties in combination of other anti-fungal agents.Candida Albicans is one of the targets of the lactoferricin B.